title: Effect of lutein on retinal neurons and oxidative stress in a model of acute retinal ischemia/reperfusion.
abstract: OBJECTIVE
  Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present study is to investigate the neuroprotective effect of lutein on retinal neurons after acute I/R injury.
  
  
  METHODS
  Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR).
  
  
  RESULTS
  In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In lutein-treated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen.
  
  
  CONCLUSIONS
  The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage.
authors.affiliation: Eye Institute, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
authors.forename: Suk-Yee
authors.initials: SY
authors.lastname: Li
authors.forename: Zhong-Jie
authors.initials: ZJ
authors.lastname: Fu
authors.forename: Huan
authors.initials: H
authors.lastname: Ma
authors.forename: Wai-Chi
authors.initials: WC
authors.lastname: Jang
authors.forename: Kwok-Fai
authors.initials: KF
authors.lastname: So
authors.forename: David
authors.initials: D
authors.lastname: Wong
authors.forename: Amy C Y
authors.initials: AC
authors.lastname: Lo
mesh_terms: D000208:Acute Disease; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis; D064032:Calbindin 2; D004195:Disease Models, Animal; D020287:In Situ Nick-End Labeling; D014975:Lutein / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects*; D011064:Poly Adenosine Diphosphate Ribose / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012164:Retinal Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012165:Retinal Ganglion Cells / Q000187:drug effects* / Q000473:pathology; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D000975:Antioxidants; D064032:Calbindin 2; D018696:Neuroprotective Agents; D064030:S100 Calcium Binding Protein G; D011064:Poly Adenosine Diphosphate Ribose; C002744:3-nitrotyrosine; D014443:Tyrosine; D014975:Lutein